Recently, hepcidin expression in adipose tissue has been described and shown to be increased in patients with severe obesity. We tried to assess the effect of obesity on hepcidin serum levels and treatment outcome of iron deficiency anemia in children. Methods This was a case control study included 70 children with iron deficiency anemia "IDA" (35 obese and 35 non-obese) and 30 healthy non-obese children with comparable age and sex(control group). Parameters of iron status (Serum iron, ferritin, transferrin, total iron binding capacity and transferrin saturation) and serum hepcidin levels were assessed initially and after 3 months of oral iron therapy for IDA. Results Compared to the control group, serum hepcidin was significantly lower in non-obese children with IDA(p < 0.01) and significantly higher in obese children with IDA (p < 0.01). Hepcidin increased significantly in non-obese children with IDA after 3 months of iron therapy (P < 0.01). On the other hand, obese children showed non-significant change in hepcidin level after iron therapy (p > 0.05). Although hepcidin showed significant positive correlations with Hb, serum iron and transferrin saturation in non-obese children with IDA, it showed significant negative correlations with Hb, serum iron and transferrin saturation in obese children with IDA (P < 0.05). Conclusions Obesity increased hepcidin levels and was associated with diminished response to oral iron therapy in childhood iron deficiency anemia.

Abstract Background:Recently, hepcidin expression in adipose tissue has been described and shown to be increased in patients with severe obesity. We tried to assess the effect of obesity on hepcidin serum levels and treatment outcome of iron deficiency anemia in children. Methods:This was a case control study included 70 children with iron deficiency anemia“IDA”(35 obese and 35 nonobese) and 30 healthy nonobese children with comparable age and sex(control group). Parameters of iron status (Serum iron, ferritin, transferrin, total iron binding capacity and transferrin saturation) and serum hepcidin levels were assessed initially and after 3 months of oral iron therapy for IDA. Results:Compared to the control group, serum hepcidin was significantly lower in nonobese children with IDA(p < 0.01) and significantly higher in obese children with IDA (p < 0.01). Hepcidin increased significantly in nonobese children with IDA after 3 months of iron therapy (P < 0.01). On the other hand, obese children showed non significant change in hepcidin level after iron therapy (p > 0.05). Although hepcidin showed significant positive correlations with Hb, serum iron and transferrin saturation in nonobese children with IDA, it showed significant negative correlations with Hb, serum iron and transferrin saturation in obese children with IDA (P < 0.05). Conclusions:Obesity increased hepcidin levels and was associated with diminished response to oral iron therapy in childhood iron deficiency anemia. Keywords:Obesity, Hepcidin, Iron deficiency, Children

Background Obesity is associated with lowserum iron concentra tions. The inverse relationship between iron status and adiposity was first reported in 1962, when Wenzel et al [1] unexpectedly found a significantly lower mean serum iron concentration in obese compared with non obese adolescents. Most subsequent studies in pediatric and adult samples have shown similar results [25]. The etiology of the hypoferremia of obesity is uncer tain. Among the proposed causes are deficient iron intake from an iron poor diet [2], and deficient iron stores owing to greater iron requirements in obese adults because of their larger blood volume [6]. Recently, fat mass was described as a significant negative

* Correspondence: zanad_zanad2005@yahoo.com 1 Department of Pediatrics, Faculty of Medicine, Zagazig University, Egypt Full list of author information is available at the end of the article

predictor of serum iron and this hypoferremia seemed not to be explained by differences in iron intake [7]. Adipose tissue is a very active endocrine organ secret ing numerous hormones and cytokines associated with important systemic effects on different metabolic pro cesses [8]. Recently, hepcidin expression in adipose tissue has been described and shown to be increased in patients with severe obesity [9]. Hepcidin is a small, cysteinerich cationic peptide produced by hepatocytes [10,11], secreted into plasma, and excreted in urine. Hepcidin expression is induced by iron stores and inflammation [11] and is suppressed by hypoxia and anemia [12]. Hep cidin is proposed to be a key regulator of iron metabo lism and its discovery has changed our understanding of the pathophysiology of iron disorders [10]. Adipose tissue of obese patients produced increased amount of